The relationship between mutagenesis and carcinogenesis is the main question addressed in this proposal. In general, carcinogens or their metabolic products, combine with DNA. The lesions which result undergo DNA repair which may result in mutations. In bacteria, many mutations are the result of an inducible, error-prone DNA repair system known as SOS repair. Error-prone (i.e. mutagenic) DNA repair pathways in animal cells exposed to UV light, and latter to chemical carcinogens, will be studied in order to see whether there is an inducible DNA repair system. Genetic, physiological and pharmacological factors which control error-prone DNA repair will be studied by measuring shifts in the mutation frequency after a standard UV fluence. The mechanism of heavy metal mutagenesis in E. coli will be analyzed by using mutants in DNA repair. Similar mutants of Chinese hamster cells will be isolated, which will allow further analysis of DNA repair pathways. It is hoped that by studying the mutation frequency in animal cells exposed to a known UV fluence, a test for co-carcinogens might be developed.